Actinobacillus pleuropneumoniae infection activates IL-1β expression in porcine alveolar macrophages via β-amyloid production.

Actinobacillus pleuropneumoniae (A. pleuropneumoniae), a porcine respiratory tract pathogen, causes porcine pleuropneumonia. Porcine alveolar macrophages (PAMs) play a crucial role during A. pleuropneumoniae infection. Amyloid precursor protein (APP) can be cleaved by β- and γ-secretase to produce β-amyloid (Aβ). APP and Aβ are associated with the inflammatory response. They activate microglia and astrocytes to secrete IL-1β, IL-6, and other cytokines. In this study, we found that during the interaction between A. pleuropneumoniae and PAMs, the two-component system CpxAR upregulates wecA expression, increasing lipopolysaccharide (LPS) production. LPS promotes APP production and cleavage to generate Aβ. The Aβ activates NF-κB, leading to increased IL-1β expression. We hypothesize that A. pleuropneumoniae infection of PAMs regulates APP production and cleavage to control Aβ levels. Different quantities of Aβ induce PAMs to produce varying amounts of cytokines, leading to different pathological processes in porcine pleuropneumonia.